Chapters (40)
- Cover Page
- Title Page
- Dedication
- Prologue A Brief History of Banting
- Part One
- Chapter 1
- Chapter 2
- Chapter 3
- Chapter 4
- Part Two
- Chapter 5
- Chapter 6
- Chapter 7
- Chapter 8
- Chapter 9
- Chapter 10
- Chapter 11
- Chapter 12
- Chapter 13
- Part Three
- Chapter 14
- Chapter 15
- Chapter 16
- Chapter 17
- Chapter 18
- Chapter 19
- Chapter 20
- Chapter 21
- Chapter 22
- Chapter 23
- Chapter 24
- Epilogue
- Notes
- Bibliography
- Acknowledgments
- Illustration Credits
- A Note About the Author
- Also by Gary Taubes
- Footnotes
- Copyright
One is Jean Mayer’s glucostat hypothesis or, technically, the glucostatic regulation of food intake, and it is invoked to explain the short-term initiation of meals. Receptors in the hypothalamus, said Mayer, metabolize glucose, initiating the sensation of hunger when the available supply of glucose falls, and provoking satiety when it rises. This glucostatic regulation, as Mayer put it, is an “essential component of the mechanism by which the needs of the body make themselves felt in the satiety centers.” It couldn’t be the only one, however, because it offered no explanation for what Mayer called “the problem of the nature of the very fine adjustment knob…the mechanism which will make you regain the weight you lost after an illness, and which makes so difficult the maintenance of weight loss after an arduous weight reduction course.”
The second hypothesis, what the Cambridge University physiologist Gordon Kennedy called lipostatic regulation or the lipostat, would evolve in the 1970s into the remarkably durable notion that we are all endowed with a certain set point of body weight or adiposity that we defend against both caloric deprivation and (perhaps less vigorously) caloric surplus. By Kennedy’s logic, the lipostat is also located in the hypothalamus and accomplishes its fine-tuning job by monitoring the amount of fat in the body or some by-product of metabolism that is released into the bloodstream in relationship to our adiposity. When this adiposity signal dips below an acceptable level—the set point—the lipostat responds by increasing food intake or decreasing energy expenditure. When the adiposity signal moves above this set point, the lipostat works to suppress food intake and perhaps increase expenditure. According to this hypothesis, the fundamental difference between the lean and the obese is the amount of fat stores that the hypothalamus is set to defend—the set point—not the manner or vigor with which it is defended. Whatever our weight, if we find ourselves in a situation where our current level of body fat is beneath that of our set point, we will fatten easily until we’ve reached our predetermined level.